Abstract
Here, we describe the production and characterization of a novel p65fl/fl/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65fl/fl/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following Salmonella infection as compared to controls. Additionally, p65fl/fl/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies.
Original language | English (US) |
---|---|
Pages (from-to) | 171-185 |
Number of pages | 15 |
Journal | Innate Immunity |
Volume | 29 |
Issue number | 8 |
DOIs | |
State | Published - Nov 2023 |
Keywords
- Animal model
- bone marrow-derived macrophage
- cytokine
- innate immunity
- nuclear factor-kappaB
ASJC Scopus subject areas
- Microbiology
- Immunology
- Molecular Biology
- Cell Biology
- Infectious Diseases